Abstrakt

Proces odbudowy uszkodzonych mięśni szkieletowych obejmuje cztery fazy: degeneracji, odpowiedzi zapalnej i immunologicznej, regeneracji oraz reorganizacji, regulowanych przez wiele cząsteczek o charakterze immuno-endokrynnym oddziałujących na komórki mięśniowe oraz komórki macierzyste mięśni. Do tych cząsteczek należy testosteron (T), który wiążąc się z wewnątrzkomórkowym receptorem androgenowym inicjuje ekspresję mięśniowej izoformy insulinopodobnego czynnika wzrostu 1 (IGF-1Ec). Współdziałanie T i IGF-1Ec stymuluje wzrost i regenerację mięśni z powodu zahamowania apoptozy, nasilenia proliferacji i różnicowania SCs. W wyniku starzenia się, dystrofii mięśniowych lub chorób wyniszczających liczba SCs ulega znacznemu obniżeniu. Regularny wysiłek fizyczny zapobiega jej obniżeniu i tym samym podwyższa potencjał regeneracyjny mięśni zarówno u młodych, jak i starszych osób. Jednym z wyzwań współczesnej medycyny jest możliwość wykorzystania komórek macierzystych oraz podłoży imitujących macierz zewnątrzkomórkową w medycynie regeneracyjnej i molekularnej, zwłaszcza w chorobach degeneracyjnych i pourazowej rekonstrukcji mięśni szkieletowych. Celem pracy jest przedstawienie aktualnych informacji na temat molekularnych i komórkowych mechanizmów regeneracji mięśni szkieletowych, roli testosteronu i czynników wzrostu w aktywacji SCs oraz możliwości ich terapeutycznego wykorzystania w stymulacji odbudowy uszkodzonych włókien mięśniowych.

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